Methods :
The vitreous from patients with retinal detachment was analyzed by quantitative metabolics. A rat model of retinal detachment and cultured photoreceptors subjected to oxidative stress were also employed to interrogate underlying molecular mechanisms.

Results :
Key metabolites in the glycolytic pathway were dysregulated in the vitreous of patients with retinal detachment. In the animal models, We showed that retinal detachment activated dynamin-related protein 1 dependent mitochondrial fission, ROS release and apoptotic cascades. Pharmacological blockade or RNA interference of dynamin-related protein 1 activity preserved mitochondrial integrity, attenuated ROS production and rescued photoreceptors both in vivo and in vitro.